Figure 4.

Effect of Janus kinase (JAK) inhibition on reverse priming of reactive oxygen species (ROS) production. The priming effect of granulocyte–macrophage‐colony stimulating factor (GM‐CSF) (5 ng/ml) on neutrophils from healthy controls (a) and RA patients (c) stimulated with f‐Met‐Leu‐Phe (fMLP) (10⁻⁸ M) decreased to ∼40% of the levels observed at 45 min, following a further 120 min in culture. Baricitinib (200 ng/ml) enhanced significantly the depriming of healthy control neutrophils after 30 and 60 min incubation (a, *P < 0·05; **P < 0·01, n = 3), but was not able to reverse GM‐CSF priming of rheumatoid arthritis (RA) neutrophils (c). Tofacitinib was not able to reverse prime GM‐CSF‐treated neutrophils from controls (a,b) or RA patients (c,d). No significant reverse priming effect was seen with either JAK inhibitor in phorbol‐12‐myristate‐12‐acetate (PMA)‐treated (100 ng/ml) neutrophils from healthy controls (b) or RA patients (d).